Half of all heart attack victims die after their first attack. The other half, more often than not, wander the earth in an imitation of life, popping pills and practising self denial. Heart attacks are scary, and the average victim doesn't want a repeat. On this basis, many feel grateful for the bewildering array of pills vasodilators, antiarrhythmics, antihypertensives, diuretics and cholesterol drugs and surgical techniques which are on offer. Some patients as well as doctors invest these things with magic, life giving potential, though there is little evidence of this.

While early mortality from heart attacks death within the first 15 days to a year depending on which study you read appears to be on the decline, the incidence of heart failure is increasing (Lancet, 1993; 341: 733-36). In US about 1 per cent of the population is having a heart attack at any one time (Cardiol Clin, 1989; 7: 1-9). In the UK about 1 million patients per year currently receive treatment for heart attacks. The question is, is it doing any good?

Each week whole forests are laid to waste reporting what we now know about heart disease. Yet the function of many heart drugs, indeed what causes heart attacks in the first place, is still not well understood. The standard risk factors smoking, high blood pressure and cholesterol account for only 50 per cent of total risks (JAMA, February 24, 1993). Because of this a wide ranging approach to heart health is likely to yield the most promising results. When considering lifestyle modifications this is a sound principle. When considering drug therapy and/or surgery it could be fatal.

A single drug can act in several different ways, sometimes unpredictably. Trials have shown that combining drugs can be fatal. For example, in trials where enalapril (an ACE inhibitor) or hydralazine (a vasodilator/antihypertensive) and isosorbide dinitrate (also a vasodilator) when added to digoxin (a glycoside to increase the force of the heart beat) and used in combination with diuretics (to treat hypertension) survival rates did improve but not by much. Within four years more than 40 per cent of the patients enrolled in these trials were dead (N Eng J Med, 1987; 316: 1429-35; N Eng J Med, 1991; 325: 293-302; N Eng J Med, 1991; 325: 303-10; N Eng J Med, 1986; 314: 1547-52).

One long term trial in Finland showed that patients on the receiving end of multiple interventions were actually more likely to die from heart failure than those who received no interventions (JAMA, 1991; 266: 1225-9). Another trial in Gottenburg following 10,000 middle aged men for 10 years showed no reduction in mortality from a multiple intervention programme (Eur Heart J, 1986; 7: 279-88). Another trial of more than 12,000 men showed similar results (JAMA, 1982; 248: 1465-77; JAMA, 1990; 263: 1795-801), as did a World Health Organization study of 61,000 men (Lancet, 1986; i: 869-72). In fact, in the British arm of the WHO study the death rate from heart disease was 8 per cent higher in the intervention group (Lancet, 1983; i: 1062-6).

Indeed, the latest study from North America demonstrates that this get in there early aggressive intervention doesn't do one bit of good. The study, which compared the use of cardiac procedures and mortality rates of more than a quarter of a million elderly patients in both Canada and the US, found that America had strikingly higher rates of aggressive cardiac treatment than Canada: 11 times the rate of angioplasty, and 10 times the rate of bypass surgery. Although short term mortality after a heart attack was slightly lower initially (21 per cent versus 22 per cent), this small gap was closed after a year. In the long term, survival rates were virtually identical between the two countries (New Eng J Med, 1997; 336: 1500-5).